The signaling protein, Stat5 plays a key role in the cancer growth.Researchers at Jefferson's Kimmel Cancer Center in Philadelphia have found that blocking Stat5 may inhibit tumor development.
The study, led by Marja Nevalainen, M.D., Ph.D., associate professor of Cancer Biology at Jefferson Medical College of Thomas Jefferson University, showed that prostate cancer cells could be effectively killed in both the laboratory and in experimental animal models by blocking the protein, Stat5.
The study demonstrated that Stat5 is both vital to prostate cancer cell maintenance and that it is a viable target for drug therapy.
The researchers wanted to prove that Stat5 was indeed necessary for prostate cancer cells to be viable, for which they blocked the protein's expression and function in several ways, including siRNA inhibition, antisense inhibition and adenoviral gene delivery of an inhibitory form of Stat5.
All of these techniques killed the prostate cancer cells in cell culture.
The researchers also showed when they transplanted such cancerous tissue into mice and blocked Stat5 expression, prostate tumors failed to grow.
"This provides the proof of principle that Stat5 is a therapeutic target protein for prostate cancer, and may be specifically useful for advanced prostate cancer, where there are no effective therapies. These results are very reproducible," Dr. Nevalainen said.
Dr. Nevalainen noted that the findings are particularly relevant because her team worked with urologists to get human prostate cancer tissue specimens from surgeries, putting them into cell tissue cultures.
She said that way the hypothesis could be tested in real human prostate cancer tissue specimens.
While the researchers are still working on establishing Stat5 as a therapeutic target for hormone-resistant prostate cancer, they are also testing whether or not blocking Stat5 can make prostate cancer cells more sensitive to other treatments, such as radiation and chemotherapy.
Dr. Nevalainen said that the next is to find pharmacological agents that inhibit the protein.
The study is published in the journal Clinical Cancer Research.